Nucleic Acids Research, 1989, Vol. 17, No. 8 3037-3048
© 1989
MOLECULAR BIOLOGY |
Complementation of adenovirus E4 mutants by transient expression of E4 cDNA and deletion plasmids
Department of Immunology and Infectious Diseases, The Johns Hopkins University School of Hygiene and Public Health Baltimore, MD 21205, USA 1Department of Biology, The Johns Hopkins University Baltimore, MD 21218 USA 2Department of Medical Genetics, University of Uppsala Biomedical Center Uppsala, Sweden
*To whom correspondence should be addressed
Received January 12, 1989. Revised March 13, 1989. Accepted March 13, 1989.
Human adenovirus mutants that carry a large deletion in early region 4 (E4) are severely defective in the synthesis of viral late proteins. Plasmids that carry intact E4 sequences can complement the late protein synthetic defect of such mutants when introduced into infected cells by transfection, presumably due to the transient expression of E4 products. Cells transfected with cDNA clones capable of expressing E4 open reading frame (ORF) 6, or deletion mutant clones expected to express either E4 ORF 6 or E4 ORF 3, also complement the mutants' defects. Thus, these E4 ORFs can individually satisfy the requirement for E4 products in viral late gene expression, and function effectively in the absence of other E4 products. Some E4 deletion mutants also exhibit a defect in the production of viral DNA. All of the clones that stimulate late gene expression also enhance one such mutant's ability to accumulate viral DNA. Thus, the ORF 3 and ORF 6 products are also individually sufficient to provide an E4 function necessary for normal viral DNA replication in the absence of other E4 products.
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